Hemodynamic profiles were obtained for patients with portal hypertension secondary to the Budd-Chiari syndrome who underwent mesoatrial shunting procedures. In contrast to the well-known hyperdynamic, low-resistance state of chronic cirrhosis, patients with the Budd-Chiari syndrome had normal cardiac index and systemic vascular resistance values before anesthesia and surgery. Opening the mesoatrial shunt produced a 46% (p less than 0.01) increase in cardiac index and a 38% (p less than 0.01) decrease in overall systemic vascular resistance. Right atrial pressure and pulmonary capillary wedge pressures were sharply increased--by 5.3 mm Hg and 4.7 mm Hg, respectively (p less than 0.01). A mathematical model was developed to assess the cause of the observed changes in systemic vascular resistance. The model suggests that the hemodynamic changes seen with shunt opening are unlikely to be the result of shunt effects alone and that dilatation of peripheral vascular beds is probable. Thus shunting converts the normal systemic vascular resistance and cardiac index of patients with the Budd-Chiari syndrome to the high-output, low-resistance state seen in patients with chronic cirrhosis. Although the physiology is complex, we conclude that the data are consistent with release, by the shunting process, of a systemic vasodilator.